We intend to continue our investigation of the role of PII in the regulation of the synthesis of GS by determining in what manner the glnA linked mutations suppress the repression of GS formation brought about by PII. We shall isolate mutants carrying insertions in glnB or in glnE, the structural gene for ATase in combination with the glnA linked mutation responsible for suppression of glnB3 and study in these mutants regulation of GS and of histidase,and also study in vitro the adenylylation and deadenylylation of GS isolated from such mutants. As far as yeast is concerned, we shall try to obtain mutants with altered regulation of the enzymes of arginine degradation and determine the effects of such mutations on the productton of P5C dehydrogenase. In addition we shall attempt to isolate mutants with altered effects of ammonia or the synthese of proline and arginine degrading enzymes. We shall attempt to discover the mechanism responsible for the glutamine insensitive synthesis of GS in the mutants obtained during the past year.